Objective Platelet aggregation, activation induced by bubbles is the main cause of decompression sick-ness.Clopidogrel(Clo) can decrease platelet aggregation through inhibiting the bind of fibrinogen and ADP .This study is designed to find if Clopidogrel can paly a protective role in decompression sickness and explore the intervention mechanism . Methods Totally 111 male SD rats divided into 3 groups:normal control group (n=20), decompression sickness(DCS) group(n=46), and DCS+Clo(Clopidogrel)treated decompression sickness (DCS+Clo)group(n=45).The rats in DCS and DCS+Clo group were placed in chamber and compressed to 1.5 MPa at speed of 2t/4 , the time of compression and res-idence was 4.5 min totally, then decompressed to surface at a speed of 3 m/s.The mortality and behavioral of rats were ob-served within 30 min post decompression .The pathology and the wet/dry ratio of lung , WBC and platelet counts in periph-eral blood, the expression of activated platelets , and immunohistochemical detection of lung tissue CD 41 expression were also been tested .Results We found Clo reduces the DCS mortality risk ( mortality rate:11/45 in DCS+Clo group vs 28/46 in DCS group, P<0.01).Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leu-kocyte in lung , the WBC counts and activated platelets in peripheral blood .Conclusion Clo can play a protective role in decompression sickness through reducing post-decompression platelet consumption and activation , decreasing the activation of leukocytes .

The psychiatric problem has become a global public health issue. The model of mental health service advocate that“Treatment of disease occurred in the hospital, but rehabilitation and management in the community”. This brings great challenge to the community health service center. By comparing the domestic and foreign mental health service system, this paper discusses the necessity of carrying out the standardized training of general practitioners in psychiatry and psychology.

Objective To investigate the effect of PPAR-δ on the lung injury of rats induced by hyperbaric oxygen (HBO2) exposure.Methods Sixty male Sprague-Dawley rats were randomly divided into six groups:air+vehicle, air+GW0742, and air+GSK0660, HBO2 +vehicle, HBO2 +GW0742, HBO2 +GSK0660.Lung injury was induced in rats by HBO2exposure (2.3 ATA, 100%O2, 8 h).Rats were injected with vehicle[10%DMSO in 0.3 ml NaCl 0.9%(v/v)] or GW0742 (0.3 mg/kg, ip) or GSK0660 (1 mg/kg, ip) at 1, 6 and 12 hours before either air or oxygen exposure .Protein levels in the bronchoalveolar lavage fluid ( BALF) , wet/dry ratio of the lung and the pathological changes in the lung tissue were detected 30 min after rats′egress.Results and Conclusion For the HBO2 +GW0742 group, the protein levels in BALF, the wet/dry ratio of the lung and the pathological changes in lung tissues all significantly decreased compared with those of the air group .These changes in HBO 2 +GSK0660 group tended to increase the level of lung injury .PPAR-δhas a protective effect on pulmonary oxygen toxicity induced by HBO 2 .

Objective To study the expression levels of microRNA (miR)-16 and miR-146a in rat lungs of decompres-sion sickness (DCS) caused by fast buoyancy ascent escape or diving .Methods At 0.5 h after fast buoyancy ascent es-cape or diving, the pathological changes in rat lungs and expression levels of miR-16,and miR-146a were detected by re-verse transcription-quantitive polymerase chain reaction and compared with normal control group .Results The pathological characteristics of lungs in two DCS groups were tissue damage .At 0.5 h after DCS caused by fast buoyancy ascent escape , the lung tissue expression levels of miR-16 and miR-146a did not significantly change compared with normal control and diving DCS groups ,but the rat lung tissue expression level of miR-146 a in diving DCS group was obviously increased , com-pared with normal control group .Conclusion miR-146a may play a role in post-transcriptional regulation in the process of diving DCS .

Objective To study the pathological changes of lung tissues during fast floating escape-induced decompres-sion sickness.Methods Eighty male SD rats were randomly divided into 2 groups, 60 in fast floating escape group (escape group) , and 20 in control group .Rats in the control group were only put in a cabin under the same atmospheric pressure (ATM).Rats in escape group were pressurized to 1.5 MPa by pressure air at the 2t/7 exponential rate and stayed for 4 min till decompression.Then the rats′survival rate was observed after 0.5 h, lung tissue specimens were collected from each rat, the pathological score was taken , according to the degree of lung injury and the R language was used for statistical analysis.Results The mortality rate was 50%.Lung tissues of these rats were pathologically characterized by stromal lung thickening, edema, and hyperemia.Kruskal non-parametric test analysis found a significant difference (P=0.0016) between the two groups .Nemenyi test was used in pairwise comparison .The death and survival animals in escape group compared with the control group, the scores were significantly different (P<0.05).The scores had no significant difference between the deach and survival animal in escape group .Conclusion Decompression sickness caused by fast floating es-cape can significantly damage the blood-lung barrier to cause pulmonary edema .

Objective To study the effect of nicardipine on fast floating escape induced lung injury in animal models with decompression sickness .Methods Sixty male SD rats were randomly and evenly divided into three groups:blank control, control and nicardipine groups .The nicardipine group was given nicardipine 50 mg/kg orally 0.5 h before entrance.In the control group, rats were given an equal volume of saline 0.5 h before entrance.The blank control group only stayed in the vehicle without any pressurized procedure .The air was pressurized at the 2t/7 exponential rate to 1.5 Mpa which was maintained for 4 min, and then uniformly decompressed to atmospheric pressure .The extravehicular survival and lung pathology were observed in rats after 0.5 h, IL1-βand TNF-αexpression levels were detected by ELISA , and the Caspase 3 expression in lung tissue was detected by Western blot .Results The incidence and mortality rate were 80%and 50%respectively in control group ,and 100%and 80%in the experimental group .The surviving animals in the two groups suffered from alveolar and interstitial lung hemorrhage , with widened interstitial lung .IL1-βin the experimental group was significantly higher than in the normal control group , while TNF-αhad no significant change .After nicardipine treatment pro-caspase 3 did not change significantly , but cleaved-caspase 3 increased significantly .Conclusion Nicardipine can aggravate lung injury caused by fast floating escape-induced decompression sickness if used before decompression.

Objective To investigate the effect of N-acetylcysteine ( NAC) on lung and heart injury of rats with a fast floating escape induced decompression sickness .Methods Eighty male Sprague-Dawley rats were randomly and evenly divided into four groups:control group and three NAC prevention groups .The NAC groups were treated with different doses of NAC(250, 500 or 1000 mg/kg)by intraperitoneal injection 1 h before entrance.In the control group, rats were given an equal volume of saline1h before entrance.The air was pressurized at the 2t/7 exponential rate to 1.5 MPa which was maintained for 4 min and then uniformly decompressed to atmospheric pressure .The extravehicular survival and pathological changes in the lung and heart tissue were detected 0.5 h after rat egress.Results The survival rate of rats treated with NAC 500 mg/kg(90%) was significantly higher than that of those treated with saline (65%)alone (P<0.05).There was large break and fusion in the structure of pulmonary alveolus of control group besides obvious erythrocyte exudation , cardiac muscle fibers edema ,and obvious denaturation and break .Conclusion NAC can play a protective role in rats with a fast floating escape induced decompression sickness by mitigating the injury to and inflammation of lung and heart tissue .

To compare the performance of self-inflating bag (SIB) with T-piece resuscitator (TPR) in neonatal resuscitation.Methods:This study involved the trainees participating in a Neonatal Resuscitation Simulation Camp (NRSC) organized by Shanghai First Maternity and Infant Hospital in December 2019. They were trained to provide positive pressure ventilation with the two devices on artificial lungs. Ventilation parameters including peak inspiratory pressure (PIP), positive end-expiratory pressure (PEEP), PIP in pulmonary alveoli (PIP alv), mean airway pressure (MAP), frequency, inspiratory time (Ti), tidal volume and minute ventilation volume were recorded and analyzed by independent sample t-test or rank sum test. Results:The PIP alv, PIP, oxygen flow rate, tidal volume and minute ventilation volume delivered by TPR were significantly lower than those by SIB [(17.18±1.61) vs (24.05±4.29) cmH 2O (1 cmH 2O=0.098 kPa), t=－6.87; (17.91±1.35) vs (29.97±4.50) cmH 2O, t=－14.06; (3.65±0.25) vs (6.88±1.59) L/min, t=－11.33; (15.90±1.81) vs (24.02±4.29) ml/min, t=－10.99; (664.71±88.94) vs (1 069.49±205.68) ml/min, t=－9.89; all P<0.001]. However, compared with SIB, the PEEP in pulmonary alveoli, Ti, duration of ventilation, inspiratory to expiratory ratio were increased when using TPR [(4.76(4.69-5.57) vs 0.19(0.12-4.10) cmH 2O, T=1 190.00; (0.59±0.15) vs (0.43±0.09) s, t=5.01; (1.46±0.23) vs (1.36±0.11) s, t=2.15; 0.71±0.22 vs 0.47±0.13, t=5.14; all P<0.05]. Conclusion:TPR could deliver more stable and safer PIP, PEEP and tidal volume than SIB and keeping MAP at a stable level during positive pressure ventilation on artificial lungs.

Objective To explore the changes and significane of USP20 and HIF-α expression in breast cancer.Methods Following transfection of shRNA-USP20 lentivirus into breast cancer MDA-MB-231 cells,the gene and protein expression levels of USP20 were detected using fluorescence quantitative PCR and Western Blot.Subsequently,the overexpression of USP20 was observed to determine its effect on HIF-α expression.Similarly,siRNA-USP20 was used to knock down USP20 in breast cancer MDA-MB-231 cells,followed by detection of gene and protein expression levels using fluorescence quantitative PCR and Western Blot.The subsequent changes in HIF-α expression were then examined.Rusults The positive expression rates of USP20 and HIF-α in breast cancer tissues were 69.6%and 46.83%,respectively,while they were negatively expressed in the adjacent normal tissues,with statistically significant differences(P＜0.01).The positive expressions of USP20 and HIF-α were predomi-nantly observed in the cytoplasm of breast cancer tissue,with a smaller amount present in the nucleus.There was a significant positive correlation between USP20 and HIF-α in breast cancer.Following transfection of shRNA-USP20 lentivirus into MDA-MB-231 cells,both the protein and gene expression levels of USP20 significantly increased(P＜0.01).Over-expression of USP20 did not affect HIF-α mRNA levels but led to a significant increase in HIF-α protein expression(P＜0.01).Conversely,siRNA-USP20 interference resulted in a significant decrease in both the protein and gene expression levels of USP20(P＜0.01),without affecting HIF-α mRNA levels;however,it caused a notable reduction in HIF-α protein expression(P＜0.01).Conclusion The expression of USP20 exhib-ited a significant positive correlation with HIF-α in breast cancer.Overexpression of USP20 led to a substantial increase in HIF-α protein expression,while knock-down of the USP20 gene resulted in a significant decrease in HIF-α protein levels.Therefore,it can be inferred that USP20 may exert its influence on the development of breast cancer through modulation of HIF-α expression,thereby providing crucial experimental evidence for clinical treat-ment,prognosis,and further investigations.